muscles Flashcards

1
Q

what muscls are voluntary

A

skeletal

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2
Q

which muscles are involuntary

A

smooth and cardiac

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3
Q

features of skeletal muscles

A

elongated cells
multiple nuclei
visible striations

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4
Q

cardiac muscle features

A

branched cels
single or double nuclei
visible triations

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5
Q

smooth muscle features

A

spindle cells
single central nuclei
no striations

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6
Q

how does endothelum-dependent vasular relaxation work?

A
vessel walls are innervated by nerves
parasympathetic released bradykinin/acetylcholine
Ca flows into endothelial cell
activates nitrix oxide synthase 
diffuses into the cell
causes activation to make GTP and GMP
calcium is taken back up
cell relaxes
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7
Q

briefly describe how smooth muscle relaxes

A
Ca in
activates bigger store
activates calmodulin
binds to it
phosphryates myosin chain kinase
kinase phosphoryates myosin head 
power stroke
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8
Q

briefly describe smooth mucle relxation

A

calcium removed from cytosol
ATP depenent pump
ATPase decrease
no muscle tension

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9
Q

how domyocardial cells work

A

elecrical impulse sprads through intercollated disks
the pulse triggers electrogenic pups to open allowing Na in
negative potential to positive
influx of Na and Ca
plateau short

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10
Q

what is excitation contraction coupling

A

Ca in through L type channels in T tubules
calcium induced calcium receptors open using RYR
Ca interacts with tropnin revealing binding sites
ca reabsorbed by SERCA and pumups
unbinds from troponin and sarcomere goes back to rest

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11
Q

what is SERCA

A

sarco-endopasmic reticulum Calcium ATPase

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12
Q

define epimysium

A

connective tissue around muscle

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13
Q

define fasciles

A

bundles of muscle fibres within the epimysium

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14
Q

define perimysium

A

connective tissue around fascicles

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15
Q

define endomysium

A

indivual myofibre muscle cells surrounded by connective tissue

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16
Q

define sarcolemma

A

plasam membrane of skeletal muscle

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17
Q

define T-tubule

A

invagination allowing electrical impulses deep into the muscules

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18
Q

define sarcoplsmic reticulum SR

A

surronds each myofibril ear the tubule

key calcium store

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19
Q

define triad

A

where the sarcoplasmic reticulum meets the T tubule

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20
Q

define the A band

A

dark

thick filaments only

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21
Q

define the I band

A

light
thin filaments only
length increases during contraction

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22
Q

define the Z line

A

intersects the I band
filaments attach here
separates adjacent sarcomeres
adheres everything. transmits the force from one sarcomere to another

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23
Q

define the H zone

A

length decreases during contraction

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24
Q

define the M line

A

middle of the A band

thick filaments attach to here

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25
what is a motor unit?
a motor neuron and all the myofibrils it innervates
26
how can motos unit size vary?
for fine control there are smaller motor units | larger muscles however use large motor units for more force in movement
27
what is the presynaptic terminal?
the nerve fibre | vesicles containing neurotranmitters are found here to be releseased
28
how wide is the synpatic celft?
20-30nm wide
29
what neurotransitter is used at the NMJ
acetylcholine Ach
30
what is a voltage gated calcium channels
found on the presynaptic membrane of the neurone when action potentaisl go across the membrane thee channels open allowing calcium into the syanptic space and to the nerve terminal
31
how do vesicles release theor contents across the cleft?
exocytosis
32
what is an acetylcholine receptor made up of?
2 alpha subunits 1 beta 1 gamma 1 delta
33
what opens Ach gates?
2 Ach molecules attaching to the 2 alpha subunits
34
describe the process of action potentials moving from the nerve to the muscles
1. arrival of action potential at the synapse causes a Ca influx due to opening of voltage gated channels 2. causes Ach vesicles to move to presynpase membrane and be released via excytosis diffusing across the cleft 3. they bind Ach receptors on muscle membrane depolarization spreads out to other parts of the muscle
35
what is EPP/ what causes it
end plate potential is made when the muscle depolarises influx of Na in the muscle leads to the initiation of it
36
what is the end plate potential
creates a local positive potential as sodium moves into the muscle fibre the end plate creates an action potential that can then spread along the muscle membrane causing contraction
37
what breaks down Ach
acetylcholinersterase into Acetyl CoA and choline | these are then taken back up by the presynaptic terminal where its synthesised back into the neurotransmitter
38
what is uscle fatigue
when the muscle is overstimulated and run out of vesicles | signals are then inhibited
39
define high safety factor
each impulse reaching the NMJ is 3 times as much end plate potential needed to stimulate the fibre therefore teh NMJ is said to have this high safety factor
40
how does muscle fatigue occur?
too much stimulation of the uscle too fast leading to a reduced number of vesicles available impulses fail to be passed onto the muscle
41
what does a drug blocking the release of Ach do?
it inactivates the muscles around because there is no releace of the neurotransmitter muscles cannot contract anymore
42
example of a drug that blocks the release of Ach
botulinum | it fuses with the vesicles preventing exocytosis
43
how do drugs stimulate muscle through imitation of ach activity?
cause depolarisation of muscle fibres except they dont get broken back down again so their action can persist for minutes to hours they cause localised areas of depolarization of fibre at end plate constant stage of muscle spasm
44
examples of drugs immitating Ach activity
methacholine and nicotine
45
how can some drugs inactivate acetlycholinesterase
combine with it in the synaptic cleft so it cannot work | therfore with each impulse, additional Ach accumulates and stimulates the fibre repetitively
46
what is the issue with drugs that inactivate acetylcholinesterase
causes muscle spasm | if in the larynx it can cause spasm here leading to smothering and death
47
what is an example of a drug inactivating Ach-ase
diisopropyl flurophosphte effective lethal poison with military potential is effective for weeks used as a 'nerve gas poison'
48
examples of drugs that block transmission at junctions
curariform drugs
49
what do curariform drugs do
prevent the passage of impulses from the nerve ending into the muscles they compete for receptor sits, when the drug binds Ach cannot
50
theurapeutic uses of drugs which block transmission at jucntions
artifical respiration to control convulsions in tetanus | during surgery when compete muscle relaxation is needed
51
describe excitation- contraction coupling
Ach released and NMJ NA enters through Ach receptors initiating an action potential potential in T tubules alters conformation of DHP receptor DHP receptor open Ca channels Ca binds t troponin allowing actin-myosin binding myosin heads do power stroke muscle tension
52
what cant myosin be cleaved into?
LMM HMM light and heavy mereomyosin
53
what allows myosin to reach bindng sites of actin?
a hinge on the LMM and HMM parts | it can flex here
54
what are thin filaments made of
actin tropnin tropmyosin
55
what covers the binding sites on actin for myosin?
troponin
56
what is MBS
myosin binding sites on actin
57
how is actin made
its a chain of gamma actin monomers forming a polymer chain of F actin this then forms a double helix strand where two strand wrap around each other
58
what causes the cessation of contraction in muscles
muscle will keep contracting as long as it has ATP once the enrgy is depleated the muscle has to stop slowly contraction is terminated by Ca being removed
59
how is Ca remove?
Ca pump called SERCA
60
what si SERCA
Ca pump that goes against concentration gradients so required energy/ ATP
61
what happens during rigor motis
calcium cannot be taken up from the cytosol space and there is no ATpase actiity so there are high amounts of it meaning actin cant dissociate from myosin contraction cycle stuck relaxation cannot take place state of continuous contraction
62
when is ATP used in muscle contraction
- generating high emerg stage from myosin - disconecting mysin from actin - pumping Ca from cytosol back to SR
63
where can the muscles ge ATp from
glycoloysis ceratin phosphate krebs cycle
64
what is creatine hosphate
a means of storing energy | found in high energy using tissues suchas brain and skeletal muscles
65
how is creatine phosphate used
process called substrate phosphylation where ATP is made
66
how is creatine used by athletes
could create greater energy reserves but the muscle has limits creatine storage uses are unknown so far
67
howis glycogen used by musce=les
broken down into a form of glucose without any oxygen required
68
how do muscles get oxygen
blood | or stored in myoglobin
69
what is mypglobin
protein found in muscles for oxygen and iron binding Myoglobin increases the solubility of oxygen. Myoglobin facilitates oxygen diffusion
70
what does high pH do to haemoaglobin
low H+ promotes tigher binding of oxgen curve to left
71
whatdt does low pH do to haemoaglobin?
higher H+ permites easier release of oxygen curve to right
72
what happens to lactic acid?
absorbed by theliver | converted into pyruvate ad glucose
73
how is oxygen used in revocery afte exercise
replenish oxymoyglobin | metabolise fatty acids in the krebs cycle to make energy
74
how is energy used in recover after exercise
restore levelss of phospcreatine | syntehsiese glycogen from absorved glucose
75
red muscle
oxidative
76
white muscle
glycolytic
77
features of oxidative red muscle
``` small high mitochondra ATP made slow contractions red due to high myoglobin ```
78
what type of contraction do red muscle have
ssustained every and can maintain contraction for long times contractio is slower
79
where are red muscles found?
postural muscles
80
features of white glycolytic muscle
bigger muscles low mitochondrai less dense and light colour uses glycogen rather than moyglobin
81
how do white glycoloytic muscle contract
hugh amount of power | but easily fatigued
82
types of rd muscle
fast and slow twitch oxidative muscles
83
what is myosin isoform I
slow twitch oxidative red muscle
84
what is moysin isoform type IIA
fast twitch oxidative glycolytic red muscle
85
what is myosin isoform IIB
fast twitch glycolitic white muscle
86
whats the difference between slow twitch oxidative red muscle and fast twitch oxidative glycolyitic red msucle
slow is oxidative and aerobic | fast oxidative glyolytic is glycolytic but becomes more oxidative with endurance training